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February 14, 2015AJP Heart and Circulatory Physiology49 citations

Modulation of angiotensin II signaling following exercise training in heart failure

IZIrving H. ZuckerHSHarold D. SchultzKPKaushik P. Patel

Key Result

Exercise training in chronic heart failure may modulate angiotensin II and sympatho-excitation interactions by reducing oxidative stress, increasing nitric oxide, and reducing ANG II.

Structured PICO

How does exercise training modulate angiotensin II signaling and sympatho-excitation in chronic heart failure?

P
Population
Patients with chronic heart failure (CHF) and preclinical models
I
Intervention
Exercise training (ExT)
O
Outcome
Modulation of neural interactions between ANG II and sympatho-excitation

This review highlights the potential cellular and neural mechanisms by which exercise training reduces sympatho-excitation and modulates angiotensin II signaling in chronic heart failure.

Abstract

Sympathetic activation is a consistent finding in the chronic heart failure (CHF) state. Current therapy for CHF targets the renin-angiotensin II (ANG II) and adrenergic systems. Angiotensin converting enzyme (ACE) inhibitors and ANG II receptor blockers are standard treatments along with β-adrenergic blockade. However, the mortality and morbidity of this disease is still extremely high, even with good medical management. Exercise training (ExT) is currently being used in many centers as an adjunctive therapy for CHF. Clinical studies have shown that ExT is a safe, effective, and inexpensive way to improve quality of life, work capacity, and longevity in patients with CHF. This review discusses the potential neural interactions between ANG II and sympatho-excitation in CHF and the modulation of this interaction by ExT. We briefly review the current understanding of the modulation of the angiotensin type 1 receptor in sympatho-excitatory areas of the brain and in the periphery (i.e., in the carotid body and skeletal muscle). We discuss possible cellular mechanisms by which ExT may impact the sympatho-excitatory process by reducing oxidative stress, increasing nitric oxide. and reducing ANG II. We also discuss the potential role of ACE2 and Ang 1-7 in the sympathetic response to ExT. Fruitful areas of further investigation are the role and mechanisms by which pre-sympathetic neuronal metabolic activity in response to individual bouts of exercise regulate redox mechanisms and discharge at rest in CHF and other sympatho-excitatory states.

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Cite This Study

Zucker et al. (2015) conducted a review in chronic heart failure (CHF). Exercise training (ExT) was evaluated. Exercise training in chronic heart failure may modulate angiotensin II and sympatho-excitation interactions by reducing oxidative stress, increasing nitric oxide, and reducing ANG II.

synapsesocial.com/papers/6a19bb6b443d3ecd7cdef1c3https://doi.org/10.1152/ajpheart.00026.2015
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